ABSTRACT
PURPOSE: Diesel exhaust particles (DEPs) can induce and trigger airway hyperresponsiveness (AHR) and inflammation. The aim of this study was to investigate the effect of long-term DEP exposure on AHR, inflammation, lung fibrosis, and goblet cell hyperplasia in a mouse model. METHODS: BALB/c mice were exposed to DEPs 1 hour a day for 5 days a week for 3 months in a closed-system chamber attached to a ultrasonic nebulizer (low dose: 100 microg/m3 DEPs, high dose: 3 mg/m3 DEPs). The control group was exposed to saline. Enhanced pause was measured as an indicator of AHR. Animals were subjected to whole-body plethysmography and then sacrificed to determine the performance of bronchoalveolar lavage and histology. RESULTS: AHR was higher in the DEP group than in the control group, and higher in the high-dose DEP than in the low-dose DEP groups at 4, 8, and 12 weeks. The numbers of neutrophils and lymphocytes were higher in the high-dose DEP group than in the low-dose DEP group and control group at 4, 8, and 12 weeks. The levels of interleukin (IL)-5, IL-13, and interferon-gamma were higher in the low-dose DEP group than in the control group at 12 weeks. The level of IL-10 was higher in the high-dose DEP group than in the control group at 12 weeks. The level of vascular endothelial growth factor was higher in the low-dose and high-dose DEP groups than in the control group at 12 weeks. The level of IL-6 was higher in the low-dose DEP group than in the control group at 12 weeks. The level of transforming growth factor-beta was higher in the high-dose DEP group than in the control group at 4, 8, and 12 weeks. The collagen content and lung fibrosis in lung tissue was higher in the high-dose DEP group at 8 and 12 weeks. CONCLUSIONS: These results suggest that long-term DEP exposure may increase AHR, inflammation, lung fibrosis, and goblet cell hyperplasia in a mouse model.
Subject(s)
Animals , Mice , Airway Remodeling , Bronchoalveolar Lavage , Collagen , Fibrosis , Goblet Cells , Hyperplasia , Inflammation , Interferon-gamma , Interleukin-10 , Interleukin-13 , Interleukin-6 , Interleukins , Lung , Lymphocytes , Nebulizers and Vaporizers , Neutrophils , Plethysmography , Pneumonia , Ultrasonics , Vascular Endothelial Growth Factor A , Vehicle EmissionsABSTRACT
Diesel exhaust particles (DEP) contain elemental carbon, organic compounds including Polyaromatic hydrocarbons (PAHs), metals, and other trace compounds. Diesel exhaust is complex mixture of thousands of chemicals. Over forty air contaminants are recognized as toxicants, such as carcinogens. Most diesel exhaust particles have aerodynamic diameters falling within a range of 0.1 to 0.25 microm. DEP was classified as a definite human carcinogen (group 1) by the International Agency for Research on Cancer at 2012 based on recently sufficient epidemiological evidence for lung cancer. Significant decreases in DEP and other diesel exhaust constituents will not be evident immediately, and outworn diesel car having longer mileage still threatens health of people in spite of recent remarkable development in diesel engine technology. Policy change in South Korea, such as introduction of diesel taxi, may raise health risk of air pollution in metropolitan area with these limitations of diesel engine. To protect people against DEP in South Korea, progressive strategies are needed, including disallowance of diesel taxi, more strict regulation of diesel engine emission, obligatory diesel particulate filter attachment in outworn diesel car, and close monitoring about health effects of DEP.
Subject(s)
Humans , Air Pollution , Carbon , Carcinogens , Hydrocarbons , International Agencies , Korea , Lung Neoplasms , Metals , Vehicle EmissionsABSTRACT
Objective To observe the toxicity of diesel exhaust particles extracts(DEPE) on V79 cell in cell viability, membrane and oxidative stress. Methods Cell exposed different concentrations of DEPE for different time , the change of cell viability, the leakage of intracellular lactate dehydrogenase(LDH), intracellular glutathione(GSH) and glutathione peroxidase (GPX)content were determined respectively, and analyzed the relation between GSH and GPX. Results The results showed that the viability of V79 cell decreased and the leakage rate of lactate dehydrogenase increased gradually in according with the increasing dosage of DEPE,and that DEPE could impair V79 cell by oxidative stress, included intracellular GSH content decreased and the activity of GPX increased, indicating that GPX might play a important role in DEPE induced GSH depletion. Conclusion DEPE may impair cell viability and the cell membrane integrity, also impair cell by oxidative stress.